Malignant ascites increases the antioxidant ability of human ovarian (SKOV-3) and gastric adenocarcinoma (KATO-III) cells

The antioxidant status of cancer cells is an important factor in tumor invasion and metastases. This study investigated whether metastatic cancer cells derive beneficial antioxidant protection from ascitic fluid and are rendered resistant to oxidative stress in the form of a chemically generated fre...

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Veröffentlicht in:Gynecologic oncology 2005-02, Vol.96 (2), p.430-438
Hauptverfasser: Yang, Wenxuan, Toffa, Samuel E., Lohn, Jonathan W.G., Seifalian, Alexander M., Winslet, Marc C.
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container_end_page 438
container_issue 2
container_start_page 430
container_title Gynecologic oncology
container_volume 96
creator Yang, Wenxuan
Toffa, Samuel E.
Lohn, Jonathan W.G.
Seifalian, Alexander M.
Winslet, Marc C.
description The antioxidant status of cancer cells is an important factor in tumor invasion and metastases. This study investigated whether metastatic cancer cells derive beneficial antioxidant protection from ascitic fluid and are rendered resistant to oxidative stress in the form of a chemically generated free radical insult. Human gastric carcinoma (KATO-III) and ovarian adenocarcinoma (SKOV-3) cell lines were cultured and incubated for 24 h with (1) M199 medium; (2) M199 + 20% fetal calf serum (FCS); (3) malignant ascites. All cells were exposed to a hydroxyl radical-generating system for 1 h. Cellular lipid peroxidation was assessed by measuring malondialdehyde (MDA) in cell suspensions. Glutathione (GSH) levels in cell pellet were measured in SKOV-3 cells after 0, 24, 48, and 72 h of incubation with buthionine sulphoximine (BSO). CD44 gene expression of cancer cells was analyzed by Northern blotting. The results showed that the cancer cells were rendered resistant to oxidative stress and with upregulated CD44 gene expression by components of malignant ascites. These findings suggest that malignant ascites increases the antioxidant ability of cancer cells and the potential of adhesion and invasion. Thus, determination of the nature of these putative tumor-protective components of ascites may provide targets for therapeutic intervention.
doi_str_mv 10.1016/j.ygyno.2004.10.016
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This study investigated whether metastatic cancer cells derive beneficial antioxidant protection from ascitic fluid and are rendered resistant to oxidative stress in the form of a chemically generated free radical insult. Human gastric carcinoma (KATO-III) and ovarian adenocarcinoma (SKOV-3) cell lines were cultured and incubated for 24 h with (1) M199 medium; (2) M199 + 20% fetal calf serum (FCS); (3) malignant ascites. All cells were exposed to a hydroxyl radical-generating system for 1 h. Cellular lipid peroxidation was assessed by measuring malondialdehyde (MDA) in cell suspensions. Glutathione (GSH) levels in cell pellet were measured in SKOV-3 cells after 0, 24, 48, and 72 h of incubation with buthionine sulphoximine (BSO). CD44 gene expression of cancer cells was analyzed by Northern blotting. The results showed that the cancer cells were rendered resistant to oxidative stress and with upregulated CD44 gene expression by components of malignant ascites. 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subjects Adenocarcinoma - genetics
Adenocarcinoma - metabolism
Adenocarcinoma - pathology
Antioxidant
Antioxidants - metabolism
Ascites - metabolism
Ascites - pathology
Blotting, Northern
Buthionine Sulfoximine - pharmacology
CD44
Cell Adhesion - physiology
Cell Line, Tumor
Cell Survival - drug effects
Female
Gastric cancer
Gene Expression
Glutathione
Glutathione - deficiency
Glutathione - metabolism
Humans
Hyaluronan Receptors - biosynthesis
Hyaluronan Receptors - genetics
Lipid Peroxidation
Malignant ascites
Malondialdehyde - metabolism
Metastases
Ovarian cancer
Ovarian Neoplasms - genetics
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Oxidative Stress
Stomach Neoplasms - genetics
Stomach Neoplasms - metabolism
Stomach Neoplasms - pathology
title Malignant ascites increases the antioxidant ability of human ovarian (SKOV-3) and gastric adenocarcinoma (KATO-III) cells
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